Difficult caesarean section: A literature review.

BACKGROUND: Caesarean section (CS) is usually perceived as a simple and safe alternative to natural birth, but in some instances can be technically difficult with consequent health hazards for both the mother and the fetus. We have proposed an evidence-based literature review of the most common difficult CS scenarios, with the aim to provide useful information about their management, possible prevention and resolution of complications. METHODS: We identified articles through a reserch in PubMed, Scopus, Web of Science and Ovid MEDLINE for studies published between 1979 and 2019. We included the best available evidence, such as RCTs, non-randomised controlled clinical trials, case-control studies, cohort studies, and case series. About sixty articles were included in this review, four hundred and thirty-six were excluded after reviewing the title or abstract or because they weren't in English. FINDINGS: The possible causes of "difficult" caesarean sections were divided into four categories: difficult access to the lower uterine segment; complicated fetal extraction, laceration or organ damage and abnormal placentation. CONCLUSIONS: Knowing in advance the potential technical difficulties and resulting risks allows the surgeon to plan appropriate strategies.

Non-obstetrical indications for cesarean section: a state-of-the-art review.

PURPOSE: To propose an evidence-based review on the most frequent indications for Cesarean section (CS) given by specialists in disciplines other than Obstetrics and Gynecology, with the aim of increasing consciousness about the available data in the literature and the guidelines recommendations about topics that are not frequently managed by obstetricians and gynecologists. METHODS: We analyzed hospital discharge data regarding deliveries occurred in a 10-year study period in our department to obtain the prevalence and the list of the most recurrent non-obstetrical indications for CS. A search was performed in PubMed, the Cochrane Library, SCOPUS, Web of Science and Ovid MEDLINE and only studies published in English from 1950 to 2017 were included. For indications for which no systematic reviews existed, we included the best available evidence, including guidelines of non-obstetrics scientific societies or organizations, RCTs, non-randomized controlled clinical trials, case-control studies, cohort studies, and case series. RESULTS: The rising rate of CS registered in the recent years is not justified by reduction in maternal--fetal risk or perinatal outcomes and often reflects inappropriate clinical behaviour and a wrong tendency that assimilates CS as a defensive practice. In a relevant percentage of cases, the indication to CS is given by specialists in other disciplines, even when specific guidelines do not give clear recommendation about the route of delivery. CONCLUSIONS: To refuse non-obstetrical indications for CS, when scientific support is lacking, could be a useful and safe strategy to further reduce the rate of unnecessary CS.

Knowledge of Human Cytomegalovirus Infection and Prevention in Pregnant Women: A Baseline, Operational Survey.

Currently, the only efficient way to prevent human Cytomegalovirus (HCMV) infection in pregnancy is primary prophylaxis through hygienic measures. So, we evaluated knowledge of HCMV and its prevention in a group of pregnant women. An anonymous questionnaire with multiple-choice answers was administered to all pregnant women who were followed up at the Obstetrics and Gynecology Unit of "Pugliese-Ciaccio Hospital," a third-level hospital in Catanzaro (Southern Italy), from November 2015 to March 2016. Previously prescribed serology results for HCMV were also evaluated. Three hundred and fifty women participated in the study and the results clearly demonstrated that knowledge of pregnant women about HCMV is poor. Moreover, prescribed screening procedures need to be optimized, since one out of three pregnant women has not been tested for HCMV or the screening was not performed adequately. For this reason, it is important to implement informative campaign in both pregnant women and providing physicians.

Efficacy and Safety of Non-Vitamin K Antagonist Oral Anticoagulants versus Vitamin K Antagonist Oral Anticoagulants in Patients Undergoing Radiofrequency Catheter Ablation of Atrial Fibrillation: A Meta-Analysis.

BACKGROUND: Use of the non-vitamin K antagonist oral anticoagulants (NOACs) is endorsed by current guidelines for stroke prevention in patients with atrial fibrillation (AF). However efficacy and safety of NOACs in patients undergoing catheter ablation (RFCA) of AF has not been well established yet. OBJECTIVES: To perform a meta-analysis of all studies comparing NOACs and vitamin K antagonist oral anticoagulants (VKAs) in patients undergoing RFCA. DATA SOURCES: Studies were searched for in PubMed and Google Scholar databases. STUDY ELIGIBILITY CRITERIA: Studies were considered eligible if: they evaluated the clinical impact of NOACs versus VKAs; they specifically analyzed the use of anticoagulants during periprocedural phase of RFCA; they reported clinical outcome data. STUDY APPRAISAL AND SYNTHESIS METHODS: 25 studies were selected, including 9881 cases. The summary measure used was the risk ratio (RR) with 95% confidence interval (CI). The random-effects or the fixed effect model were used to synthesize results from the selected studies. RESULTS: There was no significant difference in thromboembolic complications (RR 1.39; p=0.13). Bleeding complications were significantly lower in the NOACs-treated arm as compared to VKAs (RR=0.67, p<0.001). Interestingly, a larger number of thromboembolic events was found in the VKAs-treated arm in those studies where VKAs had been interrupted during the periprocedural phase (RR=0.68; p=ns). In this same subgroup a significantly higher incidence of both minor (RR=0.54; p=0.002) and major bleeding (RR=0.41; p=0.01) events was recorded. Conversely, the incidence of thromboembolic events in the VKAs-treated arm was significantly lower in those studies with uninterrupted periprocedural anticoagulation treatment (RR=1.89; p=0.02). LIMITATIONS: As with every meta-analysis, no patients-level data were available. CONCLUSIONS AND IMPLICATIONS: The use of NOACs in patients undergoing RFCA is safe, given the lower incidence of bleedings observed with NOACs. On the other side, periprocedural interruption of VKAs and bridging with heparin is associated with a higher bleeding rate with no significant benefit on onset of thromboembolic events.

The instantaneous wave-free ratio (iFR) for evaluation of non-culprit lesions in patients with acute coronary syndrome and multivessel disease.

BACKGROUND: Adenosine administration is currently required for evaluation of stenosis severity with fractional flow reserve (FFR). The instantaneous wave-free ratio (iFR) was recently introduced as an adenosine-free alternative in patients with stable CAD. The aim of the present study was to replicate the findings of previous iFR studies using an independent calculation algorithm and to evaluate the iFR for the assessment of non-culprit vessels in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: 53 patients with ACS (65%) and at least one non-culprit intermediate lesion and 29 (35%) with stable CAD were included. A total of 123 stenoses were evaluated with both FFR and iFR. Classification match of iFR in ACS was not inferior to stable CAD (79.5% in ACS and 84.4% in CAD; p=0.497). Accordingly, no difference was observed in iFR/FFR correlation between ACS and stable CAD (r=0.66 in ACS vs. r=0.69 in CAD). Overall, a significant correlation was found between iFR and FFR (r=0.68; p<0.001) with a good diagnostic efficiency at ROC analysis (area under the curve: 0.87). In addition, neither the localization of the stenosis within the coronary tree (p=0.147) nor the time interval from the acute event (p=0.550) significantly influenced the concordance of iFR with FFR. CONCLUSIONS: The iFR is a promising method for the assessment of non-culprit lesion severity in patients with acute coronary syndrome.

Administration of a loading dose has no additive effect on platelet aggregation during the switch from ongoing clopidogrel treatment to ticagrelor in patients with acute coronary syndrome.

BACKGROUND: Ticagrelor outperforms clopidogrel in preventing cardiovascular events in acute coronary syndrome. Despite the inclusion of a loading dose in the Platelet Inhibition and Patient Outcomes (PLATO) trial for all patients randomized to ticagrelor, it may not be necessary in patients receiving ongoing clopidogrel therapy. The aim of the present study was to assess whether a ticagrelor loading dose is associated with a further platelet inhibition during the switch from clopidogrel to ticagrelor in patients with acute coronary syndrome receiving ongoing antiplatelet treatment. METHODS AND RESULTS: Fifty patients with acute coronary syndrome receiving aspirin and clopidogrel treatment were randomly assigned to a starting dose of ticagrelor (group 1, 90 mg; group 2, 180 mg). Platelet aggregation was measured using multiple electrode aggregometry and standard light transmission aggregometry just before the switch and at 2, 6, 24, and 72 hours. No relevant difference in platelet aggregation was observed between the 2 study arms at baseline (P=0.256). Residual platelet aggregation was significantly reduced in both arms 2 hours after the first administration of ticagrelor (P<0.001 for both), with no difference in aggregation between groups (multiple electrode aggregometry, 17.6±7.2 versus 18.1±6 U; P=0.281). Similar results were observed with LTA. CONCLUSIONS: Switching from clopidogrel to ticagrelor without a reloading dose is feasible, and it does not hinder platelet aggregation inhibition in patients with acute coronary syndrome. Further prospective studies are needed to assess the clinical relevance of our findings. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01795820.

MicroRNA-1 downregulation increases connexin 43 displacement and induces ventricular tachyarrhythmias in rodent hypertrophic hearts.

Downregulation of the muscle-specific microRNA-1 (miR-1) mediates the induction of pathologic cardiac hypertrophy. Dysfunction of the gap junction protein connexin 43 (Cx43), an established miR-1 target, during cardiac hypertrophy leads to ventricular tachyarrhythmias (VT). However, it is still unknown whether miR-1 and Cx43 are interconnected in the pro-arrhythmic context of hypertrophy. Thus, in this study we investigated whether a reduction in the extent of cardiac hypertrophy could limit the pathological electrical remodeling of Cx43 and the onset of VT by modulating miR-1 levels. Wistar male rats underwent mechanical constriction of the ascending aorta to induce pathologic left ventricular hypertrophy (LVH) and afterwards were randomly assigned to receive 10mg/kg valsartan, VAL (LVH+VAL) delivered in the drinking water or placebo (LVH) for 12 weeks. Sham surgery was performed for control groups. Programmed ventricular stimulation reproducibly induced VT in LVH compared to LVH+VAL group. When compared to sham controls, rats from LVH group showed a significant decrease of miR-1 and an increase of Cx43 expression and its ERK1/2-dependent phosphorylation, which displaces Cx43 from the gap junction. Interestingly, VAL administration to rats with aortic banding significantly reduced cardiac hypertrophy and prevented miR-1 down-regulation and Cx43 up-regulation and phosphorylation. Gain- and loss-of-function experiments in neonatal cardiomyocytes (NCMs) in vitro confirmed that Cx43 is a direct target of miR-1. Accordingly, in vitro angiotensin II stimulation reduced miR-1 levels and increased Cx43 expression and phosphorylation compared to un-stimulated NCMs. Finally, in vivo miR-1 cardiac overexpression by an adenoviral vector intra-myocardial injection reduced Cx43 expression and phosphorylation in mice with isoproterenol-induced LVH. In conclusion, miR-1 regulates Cx43 expression and activity in hypertrophic cardiomyocytes in vitro and in vivo. Treatment of pressure overload-induced myocyte hypertrophy reduces the risk of life-threatening VT by normalizing miR-1 expression levels with the consequent stabilization of Cx43 expression and activity within the gap junction.